1. Field of Invention
The present invention relates to the field of medicine, and more particularly to a compound ambroxol hydrochloride composition and a preparation method therefor.
2. Related Art
Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease characteristic with airflow limitation, and the airflow limitation is not fully reversible and shows progressive development. COPD mainly involves lungs, but can also cause systemic (or referred to as extrapulmonary) adverse effects. COPD is a common respiratory tract disease. The old are susceptible to COPD because they have an airway mucociliary clearance dysfunction and a lung oxidation dysfunction as they become aged.
Tobacco smoke and other chronic irritants have effects on lungs to cause abnormal inflammatory responses in the lungs. COPD may involve airways, lung parenchyma and pulmonary vessels, manifesting development of chronic inflammation characteristic with neutrophils, macrophages, and lymphocytes infiltration. The inflammatory mediators released by these cells interact with structure cells in airways and lung parenchyma, thereby promoting the accumulation of T lymphocytes (especially CD+8) and neutrophils and eosinophils in the lung tissue, and the release of leukotriene B4 (LTB4), interleukin8 (IL-8), tumor necrosis factor-α (TNF-α) and other mediators, causing lung structural damage. COPD lung inflammation may be aggravated further and airflow may be limited due to oxidation-oxidation imbalance, protease-anti-protease imbalance, autonomic nervous system dysfunction, and increased cholinergic tone. Genetic susceptibility plays a role in the pathogenesis of COPD.
COPD is implicated with central airways, peripheral airways, lung parenchyma, and pulmonary vessels. Epithelial inflammatory cell infiltration occurs on central airways (trachea, bronchi, and bronchioles with diameter greater than 2-4 mm) surfaces, and the mucus secretion increases as the mucus gland enlarges and goblet cells increase. The chronic inflammation in the peripheral airways (bronchi and bronchioles with diameter less than 2 mm) causes airway wall damage and repeated repair processes. Airway wall structural remodeling occurs during the repair processes, collagen content increases and scar tissue is formed, all of these changes cause the airways to narrow, resulting in fixed airway obstruction.
COPD lung parenchyma involvement manifests centrilobular emphysema, which involves respiratory bronchioles, and causes lumen expansion and destruction. When the disease is mild, lesions often occur in the upper area of the lungs, and when disease progresses, it may involve the entire lungs, accompanied by the destruction of the pulmonary capillary bed.
Changes in the COPD pulmonary vessels which are characteristic with thickness increase of the blood vessel wall can occur early, which manifest intimal thickening, smooth muscle proliferation and vascular wall inflammatory cell infiltration. When secondary pulmonary heart disease is developed in the late stages, there may be multiple in situ thrombosis in pulmonary arterioles. Acute exacerbation of COPD is often complicated with deep vein thrombosis and pulmonary thromboembolism.